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SHR Neuro Krebs Kardio Lipid

Madreiter-Sokolowski, CT; Sokolowski, AA; Waldeck-Weiermair, M; Malli, R; Graier, WF.
Targeting Mitochondria to Counteract Age-Related Cellular Dysfunction.
Genes (Basel). 2018; 9(3): [OPEN ACCESS]
Web of Science PubMed PUBMED Central FullText FullText_MUG

 

Autor/innen der Med Uni Graz:
Graier Wolfgang
Madreiter-Sokolowski Corina
Malli Roland
Sokolowski Armin
Waldeck-Weiermair Markus
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Abstract:
Senescence is related to the loss of cellular homeostasis and functions, which leads to a progressive decline in physiological ability and to aging-associated diseases. Since mitochondria are essential to energy supply, cell differentiation, cell cycle control, intracellular signaling and Ca2+sequestration, fine-tuning mitochondrial activity appropriately, is a tightrope walk during aging. For instance, the mitochondrial oxidative phosphorylation (OXPHOS) ensures a supply of adenosine triphosphate (ATP), but is also the main source of potentially harmful levels of reactive oxygen species (ROS). Moreover, mitochondrial function is strongly linked to mitochondrial Ca2+homeostasis and mitochondrial shape, which undergo various alterations during aging. Since mitochondria play such a critical role in an organism's process of aging, they also offer promising targets for manipulation of senescent cellular functions. Accordingly, interventions delaying the onset of age-associated disorders involve the manipulation of mitochondrial function, including caloric restriction (CR) or exercise, as well as drugs, such as metformin, aspirin, and polyphenols. In this review, we discuss mitochondria's role in and impact on cellular aging and their potential to serve as a target for therapeutic interventions against age-related cellular dysfunction.

Find related publications in this database (Keywords)
mitochondria
aging
caloric restriction
exercise
caloric restriction mimetics
polyphenols
aspirin
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